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Biochem Biophys Res Commun. 2017 Aug 5;489(4):497-502. doi: 10.1016/j.bbrc.2017.05.180. Epub 2017 May 31.

Centrosomal MCM7 strengthens the Cep68-VHL interaction and excessive MCM7 leads to centrosome splitting resulting from increase in Cep68 ubiquitination and proteasomal degradation.

Author information

1
Savaid School of Medicine, University of Chinese Academy of Sciences, Beijing 100049, China.
2
Savaid School of Medicine, University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: yuanli@ucas.ac.cn.

Abstract

We have recently reported that Rootletin prevents Cep68 from VHL-mediated proteasomal degradation to maintain centrosome cohesion, unveiling the first underlying mechanism of a linker protein required for maintenance of centrosome cohesion. The minichromosome maintenance (MCM) proteins 2-7 have long been noticed to localize to centrosomes, but their functions at the centrosome are presently unknown. Here, we show that MCM7 directly binds to the centrosomal linker protein Cep68 in vitro and complexes with Cep68 and VHL in vivo. Absence of MCM7 weakened the interaction between Cep68 and VHL, whereas MCM7 overexpression facilitated the Cep68-VHL association. As a result of MCM7 overexpression, Cep68 was targeted for ubiquitination and proteasomal degradation, thereby rendering centrosome splitting. We propose that Cep68 protein level needs to be fine-tuned in order to ensure that its direct interactors, such as the microcephaly protein Cep215 and PCNT, function properly.

KEYWORDS:

Centrosome splitting; Cep68; MCM7; Proteasomal degradation; Ubiquitination

PMID:
28578000
DOI:
10.1016/j.bbrc.2017.05.180
[Indexed for MEDLINE]

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